AZT is a nucleoside analog drug that inhibits HIV-1 reverse transcriptase (RT). The viral enzyme can acquire AZT resistance by mutations that enhance the rate of ATP-mediated excision of the incorporated AZT. Now structural work illustrates how the AZT resistance mutations create a high-affinity binding site for ATP and thus promote excision.
- Xiongying Tu
- Kalyan Das
- Eddy Arnold